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Published on: November 16, 2016
Role of interferon in streptococcal infection in the mouse
D A Weigent1, T L Huff, J W Peterson
1Department of Microbiology, University of Texas Medical Branch, Galveston 77550.
Abstract:
In previous studies, we have shown the rapid in vitro induction of IFN gamma from human T cells by highly purified peptic extracts of M proteins from Streptococcus pyogenes. The present report extends these in vitro studies and shows that a mixture of both alpha/beta and gamma IFN were present in spleen cell homogenates after in vivo treatment with M protein wild-type (M+) or mutant (M-) S. pyogenes strains. The levels of bacterial-induced IFN were found to be greater in M+ treated animals. Additional studies in vivo showed that pretreatment of mice with heat-killed M+ S. pyogenes organisms significantly protected mice to pneumococcal infection compared to similarly treated M- or control animals (P less than 0.001). Further, antibodies to mouse IFN alpha/beta and antibodies specific to a synthetic N-terminal peptide of mouse IFN gamma enhanced the death of animals due to pneumococcal infection and blocked the protection observed in animals previously treated with heat-killed M+ organisms. Most importantly, treatment of mice with either type of IFN alone enhanced the survival of mice to levels similar to that observed by treatment with M+ organisms (P less than 0.05). The results strongly suggest that IFN can play a crucial role, directly or indirectly, in controlling infection by Streptococcus pneumoniae and perhaps other streptococci.
Insights
Streptococcus pyogenes M protein induces interferon (IFN) in mice, enhancing protection against pneumococcal infection. Interferon plays a crucial role in controlling streptococcal infections.
Area of Science:
- Immunology
- Microbiology
- Infectious Diseases
Background:
- Previous studies demonstrated Streptococcus pyogenes M protein's ability to induce interferon gamma (IFN-γ) in human T cells in vitro.
- The role of M protein in modulating the host immune response in vivo remained to be fully elucidated.
Purpose of the Study:
- To investigate the in vivo induction of interferons (IFNs) by Streptococcus pyogenes M protein.
- To determine the protective effects of M protein and IFNs against Streptococcus pneumoniae infection.
Main Methods:
- Mice were treated with wild-type (M+) or mutant (M-) S. pyogenes strains or heat-killed M+ organisms.
- Interferon levels in spleen cell homogenates were measured.
- Mice were challenged with Streptococcus pneumoniae to assess survival rates.
- Antibodies against mouse IFN-α/β and IFN-γ were used to block or enhance infection outcomes.
Main Results:
- Treatment with M+ S. pyogenes induced both IFN-α/β and IFN-γ in mice, with higher levels observed in M+ treated animals.
- Pretreatment with heat-killed M+ S. pyogenes significantly protected mice against pneumococcal infection.
- Antibodies against IFNs exacerbated pneumococcal infection and blocked M+ mediated protection.
- Administration of either IFN-α/β or IFN-γ alone enhanced survival against pneumococcal infection.
Conclusions:
- Interferon (IFN) plays a critical role in controlling Streptococcus pneumoniae infections, potentially through M protein-mediated induction.
- M protein from S. pyogenes can elicit a protective immune response against heterologous streptococcal infections via IFN induction.
- These findings suggest a broader role for IFNs in managing streptococcal infections.
